We continue to concentrate on hemopoietic defects and single-gene induced mouse anemias. We will persist in our efforts to establish specific-pathogen-free colonies of 50 existing stocks, carrying mutants congenic with an inbred strain, in the new Mammalian Genetics Laboratory, and will characterize, preserve, and improve stocks of all possible new mutants with hematologic defects identified at the Jackson Laboratory. We will pursue fine-structure genetic, developmental, and biochemical studies of mouse hemoglobins, utilizing four Hba alleles (alpha-chain structure) and three Hbb alleles (Beta-chain structure) and attacking the problem of tandem-duplicated, differentiated cistrons. We will carry on with our analysis of red-cell membrane defects in mice with hemolytic anemia and our analysis of the pleiotropic effects of anemia-causing genes, including germ-cell deficiency in Hertwig's anemic mice. BIBLIOGRAPHIC REFERENCES: Stern, R.H., E.S. Russell, and B.A. Taylor. 1976. Strain distribution and linkage relationship of a mouse embryonic hemoglobin variant. Biochem. Genet. 14:373-381. (reprints will be sent as soon as available). Blake, R.L., J.G. Hall, and E. S. Russell. 1976. Mitochondrial proline dehydrogenase deficiency in hyperprolinemic mice: genetic and enzymatic analyses. Biochem. Genet. 14: (in press).